Cited 0 time in
Expression of Insulin-Like Growth Factor 1 and Insulin-Like Growth Factor 1 Receptor is Associated with the Favorable Clinicopathologic Parameters in Small Intestinal Carcinomas
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Shin, Hyung Chan | - |
| dc.contributor.author | Bae, Young Kyung | - |
| dc.contributor.author | Gu, Mi Jin | - |
| dc.contributor.author | Jung, Eun Sun | - |
| dc.contributor.author | Oh, Young-Ha | - |
| dc.date.accessioned | 2022-07-16T09:44:24Z | - |
| dc.date.available | 2022-07-16T09:44:24Z | - |
| dc.date.issued | 2013-06 | - |
| dc.identifier.issn | 1015-2008 | - |
| dc.identifier.issn | 1423-0291 | - |
| dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/162696 | - |
| dc.description.abstract | Objective: The insulin-like growth factor (IGF) system has been known to play a critical role in tumor development and progression in many human cancers. However, the role of the IGF system in small intestinal carcinoma (SIC) has not been studied yet. Methods: We evaluated the expression of IGF1 and IGF1 receptor (IFG1R) in a total of 194 cases of SIC. Results: IGF1 expression was associated with well/moderate differentiation, better survival, lower pT, lower stage and no lymph node metastasis. IGF1R was more diffusely and strongly expressed in tumors with lower pT and lower stage. Conclusions: IGF1 and IGF1R expression is associated with favorable clinicopathologic parameters and may involve early carcinogenesis of SICs. Target therapy for the IGF1R signaling pathway may not have a major therapeutic role in treating SIC. | - |
| dc.format.extent | 6 | - |
| dc.language | 영어 | - |
| dc.language.iso | ENG | - |
| dc.publisher | S. Karger AG | - |
| dc.title | Expression of Insulin-Like Growth Factor 1 and Insulin-Like Growth Factor 1 Receptor is Associated with the Favorable Clinicopathologic Parameters in Small Intestinal Carcinomas | - |
| dc.type | Article | - |
| dc.publisher.location | 스위스 | - |
| dc.identifier.doi | 10.1159/000350309 | - |
| dc.identifier.scopusid | 2-s2.0-84877854388 | - |
| dc.identifier.wosid | 000320218800007 | - |
| dc.identifier.bibliographicCitation | Pathobiology, v.80, no.5, pp 265 - 270 | - |
| dc.citation.title | Pathobiology | - |
| dc.citation.volume | 80 | - |
| dc.citation.number | 5 | - |
| dc.citation.startPage | 265 | - |
| dc.citation.endPage | 270 | - |
| dc.type.docType | Article | - |
| dc.description.isOpenAccess | N | - |
| dc.description.journalRegisteredClass | sci | - |
| dc.description.journalRegisteredClass | scie | - |
| dc.description.journalRegisteredClass | scopus | - |
| dc.relation.journalResearchArea | Cell Biology | - |
| dc.relation.journalResearchArea | Pathology | - |
| dc.relation.journalWebOfScienceCategory | Cell Biology | - |
| dc.relation.journalWebOfScienceCategory | Pathology | - |
| dc.subject.keywordPlus | FACTOR-I RECEPTOR | - |
| dc.subject.keywordPlus | GASTROINTESTINAL-STROMAL-TUMORS | - |
| dc.subject.keywordPlus | THERAPEUTIC TARGET | - |
| dc.subject.keywordPlus | COLORECTAL-CANCER | - |
| dc.subject.keywordPlus | CELL CARCINOMA | - |
| dc.subject.keywordPlus | IGF-II | - |
| dc.subject.keywordPlus | OVEREXPRESSION | - |
| dc.subject.keywordPlus | ADENOCARCINOMA | - |
| dc.subject.keywordPlus | PHENOTYPE | - |
| dc.subject.keywordPlus | GISTS | - |
| dc.subject.keywordAuthor | Small intestine | - |
| dc.subject.keywordAuthor | Carcinoma | - |
| dc.subject.keywordAuthor | Immunohistochemistry | - |
| dc.subject.keywordAuthor | Insulin-like growth factor system | - |
| dc.subject.keywordAuthor | Insulin-like growth factor 1 | - |
| dc.subject.keywordAuthor | Insulin-like growth factor 1 receptor | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
222, Wangsimni-ro, Seongdong-gu, Seoul, 04763, Korea+82-2-2220-1366
COPYRIGHT © 2024 HANYANG UNIVERSITY.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.
